Elderly patients who receive anesthesia are no more likely to develop long-term dementia or Alzheimer’s disease than other seniors, according to new Mayo Clinic research.

The study analyzed thousands of patients using the Rochester Epidemiology Project — which allows researchers access to medical records of nearly all residents of Olmsted County, Minn. — and found that receiving general anesthesia for procedures after age 45 is not a risk factor for developing dementia. The findings were published Wednesday, May 1, online in Mayo Clinic Proceedings.

Researchers know that some elderly patients have problems with cognitive function for weeks, sometimes months, following surgical procedures, says senior author David Warner, M.D., a pediatric anesthesiologist at the Mayo Clinic Children’s Center.

There has been concern that exposure to anesthesia may be associated with long-term cognitive changes including dementia, he says. The concern stems in part from a series of studies in which animals were exposed to anesthesia and lesions similar to those observed in Alzheimer’s disease appeared in the brain — including accumulation of amyloid, a protein associated with Alzheimer’s disease.

“It’s reassuring we’re adding to the body of knowledge that there is not an association of anesthesia and surgery with Alzheimer’s,” Dr. Warner says. “There are a lot of things to worry about when an elderly person has surgery, but it seems that developing Alzheimer’s isn’t one of them.”

Researchers studied about 900 patients older than 45 who had dementia and lived in Olmsted County from 1985 to 1994. They compared that group to people of similar ages in Olmsted County who did not develop dementia during that time. Researchers found that about 70 percent of the patients in both groups needed surgery requiring general anesthesia — meaning those who had dementia and underwent surgery that included general anesthesia did not get worse, and those who did not have dementia and had surgery did not develop dementia as a result.

Mayo Clinic anesthesiologist Juraj Sprung, M.D., Ph.D., is the study’s first author. The study was funded by Mayo Clinic and the National Center for Advancing Translational Sciences.

The disrupted metabolism of sugar, fat and calcium is part of the process that causes the death of neurons in Alzheimer’s disease.

Researchers from Karolinska Institutet in Sweden have now shown, for the first time, how important parts of the nerve cell that are involved in the cell’s energy metabolism operate in the early stages of the disease. These somewhat surprising results shed new light on how neuronal metabolism relates to the development of the disease.

In the Alzheimer’s disease brain, plaques consisting of so called amyloid-beta-peptide (A?) are accumulated. It is also a well-known fact that the nerve cells of patients with Alzheimer’s disease have problems metabolising for example glucose and calcium, and that these disorders are associated with cell death. The metabolism of these substances is the job of the cell mitochondria, which serve as the cell’s power plant and supply the cell with energy.

However, for the mitochondria to do this, they need good contact with another part of the cell called the endoplasmic reticulum (ER). The specialised region of ER that is in contact with mitochondria is called the MAM region. Earlier studies on yeast and other types of cells have shown that the deactivation of certain proteins in the MAM region disrupt the contact points between the mitochondria and the ER, preventing the delivery of energy to the cell and causing cell death.

Now for the first time, researchers at Karolinska Institutet have studied the MAM region in nerve cells, and examined the interaction between the mitochondria and the ER in early stage Alzheimer’s disease. Although at this point in the development of the disease A? has not formed large, lumpy plaques, symptoms still appear, implying that A? that has not yet formed plaque is toxic to neurons.

The team’s results are slightly surprising. When nerve cells are exposed to low doses of A?, it leads to an increase in the number of contact points between the mitochondria and the ER, causing more calcium to be transferred from the ER to the mitochondria. The resulting over-accumulation of calcium is toxic to the mitochondria and affects their ability to supply energy to the nerve cell.

“It’s urgent that we find out what causes neuronal death if we’re to develop molecules that check the disease,” says Maria Ankarcrona, docent and researcher at the Department of Neurobiology, Care Sciences and Society, and the Alzheimer’s Disease Research Centre of Karolinska Institutet. “In the long run we might be able to produce a drug that can arrest the progress of the disease at a stage when the patient is still able to manage their daily lives. If we can extend that period by a number of years, we’d have made great gains. Today there are no drugs that affect the actual disease process.”

The researchers conducted their studies on mice bred to develop symptoms of Alzheimer’s disease. They also studied nerve cells from deceased Alzheimer’s patients and neurons cultivated in the laboratory.

The study was financed by grants from the Swedish Research Council, the Swedish Alzheimer Foundation, the Gamla Tjänarinnor foundation, the Stohne Foundation and the Lundbeck Foundation, and through a donation from the Peter Thelin Family.

A new hypothesis has been developed by researchers in Bochum on how Alzheimer’s disease could occur. They analysed the interaction of the proteins FE65 and BLM that regulate cell division. In the cell culture model, they discovered spherical structures in the nucleus that contained FE65 and BLM.

The interaction of the proteins triggered a wrong signal for cell division. This may explain the degeneration and death of nerve cells in Alzheimer’s patients.

The team led by Dr. Thorsten Müller and Prof. Dr. Katrin Marcus from the Department of Functional Proteomics in cooperation with the RUB’s Medical Proteome Centre headed by Prof. Helmut E. Meyer reported on the results in the “Journal of Cell Science“.

Components of spherical structures in the nucleus identified

The so-called amyloid precursor protein APP is central to Alzheimer’s disease. It spans the cell membrane, and its cleavage products are linked to protein deposits that form in Alzheimer patients outside the nerve cells. APP anchors the protein FE65 to the membrane, which was the focus of the current study. FE65 can migrate into the nucleus, where it plays a role in DNA replication and repair.

Based on cells grown in the laboratory, the team led by Dr. Müller established that FE65 can unite with other proteins in the cell nucleus to form spherical structures, so-called “nuclear spheres”. Video microscopy showed that these ring-like structures merge with each other and can thus grow. “By using a special cell culture model, we were able to identify additional components of these spheres”, says Andreas Schrötter, PhD student in the working group Morbus Alzheimer at the Institute for Functional Proteomics. Among other things, the scientists found the protein BLM, which is known from Bloom’s syndrome – an extremely rare hereditary disease, which is associated with dwarfism, immunodeficiency, and an increased risk of cancer. BLM is involved in DNA replication and repair in the nucleus.

The amount of FE65 determines the amount of BLM in the cell nucleus

Müller’s team took a closer look at the function of FE65. By means of genetic manipulation, the researchers generated cell cultures, in which the FE65-production was reduced. A smaller amount of FE65 thus generated a smaller amount of the protein BLM in the nucleus. Instead, BLM collected in another area of the cell, the endoplasmic reticulum.

In addition, the researchers found a lower rate of DNA replication in the genetically modified cells. In this way, FE65 influences the replication of the genetic material via the BLM protein. When the researchers cranked up the FE65-production again, the amount of BLM in the nucleus also increased again.

FE65 as a possible trigger for Alzheimer’s

In patients with Alzheimer’s disease, the protein APP, an interaction partner of FE65, changes. The interaction of the two molecules is important for the transport of FE65 into the nucleus, where it regulates cell division in combination with BLM. Müller’s team assumes that the altered APP-FE65 interaction mistakenly sends the cells the signal to divide. Since nerve cells normally cannot divide, they degenerate instead and die. “This hypothesis, which we pursue in the working group Morbus Alzheimer, also delivers new starting points for potential therapies, which are urgently needed for Alzheimer’s disease,” says Dr. Mueller. In the future, the team will also investigate whether and how the amount of BLM is altered in Alzheimer’s patients compared to healthy subjects.

Risk prediction tools that estimate future risk of heart disease and stroke may be more useful predictors of future decline in cognitive abilities, or memory and thinking, than a dementia risk score, according to a new study published in the April 2, 2013, print issue of Neurology®, the medical journal of the American Academy of Neurology.

“This is the first study that compares these risk scores with a dementia risk score to study decline in cognitive abilities 10 years later,” said Sara Kaffashian, PhD, with the French National Institute of Health and Medical Research (INSERM) in Paris, France.

The study involved 7,830 men and women with an average age of 55. Risk of heart disease and stroke (cardiovascular disease) and risk of dementia were calculated for each participant at the beginning of the study.

The heart disease risk score included the following risk factors: age, blood pressure, treatment for high blood pressure, high density lipoprotein (HDL) cholesterol, total cholesterol, smoking, and diabetes. The stroke risk score included age, blood pressure, treatment for high blood pressure, diabetes, smoking, history of heart disease, and presence of cardiac arrhythmia (irregular heart beat).

The dementia risk score included age, education, blood pressure, body mass index (BMI), total cholesterol, exercise, and whether a person had the APOE ?4 gene, a gene associated with dementia.

Memory and thinking abilities were measured three times over 10 years.

The study found that all three risk scores predicted 10-year decline in multiple cognitive tests. However, heart disease risk scores showed stronger links with cognitive decline than a dementia risk score. Both heart and stroke risk were associated with decline in all cognitive tests except memory; dementia risk was not linked with decline in memory and verbal fluency.

“Although the dementia and cardiovascular risk scores all predict cognitive decline starting in late middle age, cardiovascular risk scores may have an advantage over the dementia risk score for use in prevention and for targeting changeable risk factors since they are already used by many physicians. The findings also emphasize the importance of risk factors for cardiovascular disease such as high cholesterol and high blood pressure in not only increasing risk of heart disease and stroke but also having a negative impact on cognitive abilities,” said Kaffashian.

The strongest predictor of whether a man is developing dementia with Lewy bodies — the second most common form of dementia in the elderly — is whether he acts out his dreams while sleeping, Mayo Clinic researchers have discovered. Patients are five times more likely to have dementia with Lewy bodies if they experience a condition known as rapid eye movement (REM) sleep behavior disorder than if they have one of the risk factors now used to make a diagnosis, such as fluctuating cognition or hallucinations, the study found.

The findings were being presented at the annual meeting of the American Academy of Neurology in San Diego. REM sleep behavior disorder is caused by loss of the normal muscle paralysis that occurs during REM sleep. It can appear three decades or more before a diagnosis of dementia with Lewy bodies is made in males, the researchers say. The link between dementia with Lewy bodies and the sleep disorder is not as strong in women, they add.

“While it is, of course, true that not everyone who has this sleep disorder develops dementia with Lewy bodies, as many as 75 to 80 percent of men with dementia with Lewy bodies in our Mayo database did experience REM sleep behavior disorder. So it is a very powerful marker for the disease,” says lead investigator Melissa Murray, Ph.D., a neuroscientist at Mayo Clinic in Florida.

The study’s findings could improve diagnosis of this dementia, which can lead to beneficial treatment, Dr. Murray says.

“Screening for the sleep disorder in a patient with dementia could help clinicians diagnose either dementia with Lewy bodies or Alzheimer’s disease,” she says. “It can sometimes be very difficult to tell the difference between these two dementias, especially in the early stages, but we have found that only 2 to 3 percent of patients with Alzheimer’s disease have a history of this sleep disorder.”

Once the diagnosis of dementia with Lewy bodies is made, patients can use drugs that can treat cognitive issues, Dr. Murray says. No cure is currently available.

Researchers at Mayo Clinic in Minnesota and Florida, led by Dr. Murray, examined magnetic resonance imaging, or MRI, scans of the brains of 75 patients diagnosed with probable dementia with Lewy bodies. A low-to-high likelihood of dementia was made upon an autopsy examination of the brain.

The researchers checked the patients’ histories to see if the sleep disorder had been diagnosed while under Mayo care. Using this data and the brain scans, they matched a definitive diagnosis of the sleep disorder with a definite diagnosis of dementia with Lewy bodies five times more often than they could match risk factors, such as loss of brain volume, now used to aid in the diagnosis. The researchers also showed that low-probability dementia with Lewy bodies patients who did not have the sleep disorder had findings characteristic of Alzheimer’s disease.

“When there is greater certainty in the diagnosis, we can treat patients accordingly. Dementia with Lewy bodies patients who lack Alzheimer’s-like atrophy on an MRI scan are more likely to respond to therapy — certain classes of drugs — than those who have some Alzheimer’s pathology,” Dr. Murray says.

The study was supported by the National Institutes of Health/National Institute on Aging [P50-AG016574, R01-AG040042, R01-AG011378, U01-AG006786], the Harry T. Mangurian, Jr., Foundation, and the Robert H. and Clarice Smith and Abigail Van Buren Alzheimer’s Disease Research Program of the Mayo Foundation.

From the Medical College of Georgia at Georgia Regents University press release via EurekAlert!:

Women who abruptly and prematurely lose estrogen from surgical menopause have a two-fold increase in cognitive decline and dementia.

“This is what the clinical studies indicate and our animal studies looking at the underlying mechanisms back this up,” said Brann, corresponding author of the study in the journal Brain. “We wanted to find out why that is occurring. We suspect it’s due to the premature loss of estrogen.”

In an effort to mimic what occurs in women, Brann and his colleagues looked at rats 10 weeks after removal of their estrogen-producing ovaries that were either immediately started on low-dose estrogen therapy, started therapy 10 weeks later or never given estrogen.

When the researchers caused a stroke-like event in the brain’s hippocampus, a center of learning and memory, they found the rodents treated late or not at all experienced more brain damage, specifically to a region of the hippocampus called CA3 that is normally stroke-resistant.

To make matters worse, untreated or late-treated rats also began an abnormal, robust production of Alzheimer’s disease-related proteins in the CA3 region, even becoming hypersensitive to one of the most toxic of the beta amyloid proteins that are a hallmark of Alzheimer’s.

Both problems appear associated with the increased production of free radicals in the brain. In fact, when the researchers blocked the excessive production, heightened stroke sensitivity and brain cell death in the CA3 region were reduced.

Although exactly how it works is unknown, estrogen appears to help protect younger females from problems such as stroke and heart attack. Their risks of the maladies increase after menopause to about the same as males. Follow up studies are needed to see if estrogen therapy also reduces sensitivity to the beta amyloid protein in the CA3 region, as they expect, Brann noted.

Brann earlier showed that prolonged estrogen deprivation in aging rats dramatically reduces the number of brain receptors for the hormone as well as its ability to prevent strokes. Damage was forestalled if estrogen replacement was started shortly after hormone levels drop, according to the 2011 study in the journal Proceedings of the National Academy of Sciences.

The surprising results of the much-publicized Women’s Health Initiative – a 12-year study of 161,808 women ages 50-79 – found hormone therapy generally increased rather than decreased stroke risk as well as other health problems. Critics said one problem with the study was that many of the women, like Brann’s aged rats, had gone years without hormone replacement, bolstering the case that timing is everything.

“Use it or lose it.” The saying could apply especially to the brain when it comes to protecting against Alzheimer’s disease. Previous studies have shown that keeping the mind active, exercising and social interactions may help delay the onset of dementia in Alzheimer’s disease.

Now, a new study led by Dennis Selkoe, MD, co-director of the Center for Neurologic Diseases in the BWH Department of Neurology, provides specific pre-clinical scientific evidence supporting the concept that prolonged and intensive stimulation by an enriched environment, especially regular exposure to new activities, may have beneficial effects in delaying one of the key negative factors in Alzheimer’s disease.

The study was published online on March 6, 2013 in Neuron.

Alzheimer’s disease occurs when a protein called amyloid beta accumulates and forms “senile plaques” in the brain. This protein accumulation can block nerve cells in the brain from properly communicating with one another. This may gradually lead to an erosion of a person’s mental processes, such as memory, attention, and the ability to learn, understand and process information.

The BWH researchers used a wild-type mouse model when evaluating how the environment might affect Alzheimer’s disease. Unlike other pre-clinical models used in Alzheimer’s disease research, wild-type mice tend to more closely mimic the scenario of average humans developing the disease under normal environmental conditions, rather than being strongly genetically pre-disposed to the disease.

Selkoe and his team found that prolonged exposure to an enriched environment activated certain adrenalin-related brain receptors which triggered a signaling pathway that prevented amyloid beta protein from weakening the communication between nerve cells in the brain’s “memory center,” the hippocampus. The hippocampus plays an important role in both short- and long-term memory.

The ability of an enriched, novel environment to prevent amyloid beta protein from affecting the signaling strength and communication between nerve cells was seen in both young and middle-aged wild-type mice.

“This part of our work suggests that prolonged exposure to a richer, more novel environment beginning even in middle age might help protect the hippocampus from the bad effects of amyloid beta, which builds up to toxic levels in one hundred percent of Alzheimer patients,” said Selkoe.

Moreover, the scientists found that exposing the brain to novel activities in particular provided greater protection against Alzheimer’s disease than did just aerobic exercise. According to the researchers, this observation may be due to stimulation that occurred not only physically, but also mentally, when the mice moved quickly from one novel object to another.

“This work helps provide a molecular mechanism for why a richer environment can help lessen the memory-eroding effects of the build-up of amyloid beta protein with age,” said Selkoe. “They point to basic scientific reasons for the apparent lessening of AD risk in people with cognitively richer and more complex experiences during life.”

A team of European scientists from the University Medical Center Hamburg-Eppendorf (UKE) and the Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) at the University of Cologne in Germany has taken an important step closer to understanding the root cause of age-related dementia.

In research involving both worms and mice, they have found that age-related dementia is likely the result of a declining ability of neurons to dispose of unwanted aggregated proteins. As protein disposal becomes significantly less efficient with increasing age, the buildup of these unwanted proteins ultimately leads to the development and progression of dementia. This research appears in the March 2013 issue of the journal GENETICS.

“By studying disease progression in dementia, specifically by focusing on mechanisms neurons use to dispose of unwanted proteins, we show how these are interconnected and how these mechanisms deteriorate over time,” said Markus Glatzel, M.D., a researcher involved in the work from the Institute of Neuropathology at UKE in Hamburg, Germany. “This gives us a better understanding as to why dementias affect older persons; the ultimate aim is to use these insights to devise novel therapies to restore the full capacity of protein disposal in aged neurons.”

To make this discovery, scientists carried out their experiments in both worm and mouse models that had a genetically-determined dementia in which the disease was caused by protein accumulation in neurons. In the worm model, researchers in the lab of Thorsten Hoppe, Ph.D., from the CECAD Cluster of Excellence could inactivate distinct routes used for the disposal of the unwanted proteins. Results provided valuable insight into the mechanisms that neurons use to cope with protein accumulation. These pathways were then assessed in young and aged mice. This study provides an explanation of why dementias exponentially increase with age. Additionally, neuron protein disposal methods may offer a therapeutic target for the development of drugs to treat and/or prevent dementias.

“This is an exciting study that helps us understand what’s going wrong at a cellular level in age-related dementias,” said Mark Johnston, Ph.D., Editor-in-Chief of the journal GENETICS. “This research holds possibilities for future identification of substances that can prevent, stop, or reverse this cellular malfunction in humans.”

A study in the JAMA Neurology (formerly the Archives of Neurology) suggests that controlling or preventing risk factors such as hypertension earlier in life may limit or delay the brain changes associated with Alzheimer’s disease and other age-related neurological deterioration.

Dr. Karen Rodrigue, assistant professor in the UT Dallas Center for Vital Longevity (CVL), was lead author on a study that looked at whether people with both hypertension and a common gene associated with risk of Alzheimer’s disease (the APOE-4 gene carried by about 20 percent of the population) had more buildup of the brain plaque (amyloid protein) associated with Alzheimer’s disease. Many scientists believe the amyloid plaque is the first symptom of Alzheimer’s disease and shows up a decade or more before Alzheimer’s symptoms of memory impairment and other cognitive difficulties begin.

Until recently, amyloid plaque could only be seen at autopsy, but new brain scanning techniques allow scientists to see the amyloid plaque in living brains of healthy adults. Findings from both autopsy and amyloid brain scans show that at least 20 percent of normal older adults carry elevated levels of amyloid, a substance made up mostly of protein and deposited in organs and tissues.

“I became interested in whether hypertension was related to increased risk of amyloid plaques in the brains of otherwise healthy people,” Rodrigue said. “Identifying the most significant risk factors for amyloid deposition in seemingly healthy adults will be critical in advancing medical efforts aimed at prevention and early detection.”

Based on evidence that hypertension was associated with Alzheimer’s disease, Rodrigue suspected that the double-whammy of hypertension and presence of the APOE-e4 gene might lead to particularly high levels of amyloid plaque in healthy adults.

Rodrigue’s research was part of the Dallas Lifespan Brain Study, a comprehensive study of the aging brain in a large group of adults of all ages funded by the National Institute on Aging. As part of this study, the research team recruited 147 participants (ages 30-89) to undergo cognitive testing, magnetic resonance imaging (MRI) and PET imaging, using Amyvid, a compound that when injected travels to the brain and binds with amyloid proteins, allowing the scientists to visualize the amount of amyloid plaque. Blood pressure was measured at each visit.

Rodrigue classified participants in the study as hypertensive if they reported a current physician diagnosis of hypertension or if their blood pressure exceeded the established criteria for diagnosis. The participants were further divided between individuals who were taking anti-hypertensive medications and those who were not medicated, but showed blood pressure elevations consistent with a diagnosis of hypertension. Finally, study subjects were classified in the genetic risk group if they were in the 20 percent of adults who had one or two copies of an APOE ?4 allele, a genetic variation linked to dementia.

The most striking result of the study was that unmedicated hypertensive adults who also carried a genetic risk factor for Alzheimer’s disease, showed much higher amyloid levels than all other groups. Adults taking hypertensive medications, even those with genetic risk, had levels of amyloid plaque equivalent to participants without hypertension or genetic risk.

The study suggests that controlling hypertension may significantly decrease the risk of developing amyloid deposits, even in those with genetic risk, in healthy middle-aged and older adults. Rodrigue noted that long-term studies of many people were needed to be certain that it was the use of hypertensive medications that was causal of the decreased amyloid deposits. Nevertheless, this early finding provides a window into the potential benefits of controlling hypertension that goes beyond decreasing risk of strokes and other cardiovascular complications.

Scientists cannot fully explain the neural mechanisms underlying the effect of hypertension and APOE ?4 on amyloid accumulation. But earlier research in animal models showed that chronic hypertension may enable easier penetration of the blood-brain barrier, resulting in more amyloid deposition.

The recent study is significant because it focuses on a group of healthy and cognitively normal middle-aged and older adults, which enables the examination of risk factors and amyloid burden before the development of preclinical dementia. The team plans for long-term longitudinal follow-up with participants to determine which proportion of the subjects eventually develop the disease.

The study’s coauthors included Dr. Denise Park, director of the Dallas Lifespan Brain Study, and Dr. Kristen Kennedy and doctoral student Jennifer Rieck, all from The University of Texas at Dallas. The team also included Dr. Michael Devous and Dr. Ramon Diaz-Arrastia, scientists from UT Southwestern Medical Center and the Uniformed Services University of the Health Sciences. In addition to the National Institute on Aging, the Alzheimer’s Association provided funds for the study. Avid Radiopharmaceutical provided doses of Amyvid that allowed the researchers to image the amyloid plaque with a PET scan.

From the Washington University School of Medicine press release via EurekAlert!:

Sleep is disrupted in people who likely have early Alzheimer’s disease but do not yet have the memory loss or other cognitive problems characteristic of full-blown disease, researchers at Washington University School of Medicine in St. Louis report March 11 in JAMA Neurology.

The finding confirms earlier observations by some of the same researchers. Those studies showed a link in mice between sleep loss and brain plaques, a hallmark of Alzheimer’s disease. Early evidence tentatively suggests the connection may work in both directions: Alzheimer’s plaques disrupt sleep, and lack of sleep promotes Alzheimer’s plaques.

“This link may provide us with an easily detectable sign of Alzheimer’s pathology,” says senior author David M. Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of Washington University’s Department of Neurology. “As we start to treat people who have markers of early Alzheimer’s, changes in sleep in response to treatments may serve as an indicator of whether the new treatments are succeeding.”

Sleep problems are common in people who have symptomatic Alzheimer’s disease, but scientists recently have begun to suspect that they also may be an indicator of early disease. The new paper is among the first to connect early Alzheimer’s disease and sleep disruption in humans.

For the new study, researchers recruited 145 volunteers from the University’s Charles F. and Joanne Knight Alzheimer’s Disease Research Center. All of the volunteers were 45 to 75 years old and cognitively normal when they enrolled.

As a part of other research at the center, scientists already had analyzed samples of the volunteers’ spinal fluids for markers of Alzheimer’s disease. The samples showed that 32 participants had preclinical Alzheimer’s disease, meaning they were likely to have amyloid plaques present in their brains but were not yet cognitively impaired.

Participants kept daily sleep diaries for two weeks, noting the time they went to bed and got up, the number of naps taken on the previous day, and other sleep-related information.

The researchers tracked the participants’ activity levels using sensors worn on the wrist that detected the wearer’s movements.

“Most people don’t move when they’re asleep, and we developed a way to use the data we collected as a marker for whether a person was asleep or awake,” says first author Yo-El Ju, MD, assistant professor of neurology. “This let us assess sleep efficiency, which is a measure of how much time in bed is spent asleep.”

Participants who had preclinical Alzheimer’s disease had poorer sleep efficiency (80.4 percent) than people without markers of Alzheimer’s (83.7 percent). On average, those with preclinical disease were in bed as long as other participants, but they spent less time asleep. They also napped more often.

“When we looked specifically at the worst sleepers, those with a sleep efficiency lower than 75 percent, they were more than five times more likely to have preclinical Alzheimer’s disease than good sleepers,” Ju says.

Ju and her colleagues are following up with studies in younger participants who have sleep disorders.

“We think this may help us get a better feel for the way this connection flows — does sleep loss drive Alzheimer’s, does Alzheimer’s lead to sleep loss, or is it a combination?” Ju says. “That will help us determine whether we can change the course of disease with pharmaceuticals or other treatments.”